کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4432757 | 1619940 | 2007 | 15 صفحه PDF | دانلود رایگان |
We constructed a probabilistic risk-based framework to assess the human oxidative stress (OS) risk from diesel exhaust particle (DEP)-induced reactive oxygen species. A human respiratory tract model was used to estimate DEP concentration and cumulative doses in lung regions for three occupational groupings (driver, homeworker and student) in northern, central, and southern Taiwan. Dose–response profiles were reconstructed in terms of the specific ratio of the reduced and oxidized forms of glutathione (GSH/GSSG ratio) for the human macrophage cell (THP-1) and human bronchial epithelial cell (BEAS-2B). The highest estimated median daily cumulative dose of DEP with 95% CI was for driver in northern Taiwan (DEP2.5: 0.716 (0.443−1.197) mg and DEP0.18: 0.584 (0.417−0.822) mg), significantly higher than that of the other settings. The driver in northern Taiwan setting had the highest cumulative dose–response calculated over a 2-year exposure period: 0.57 (0.41–0.76) and 0.70 (0.53–0.87) for DEP2.5 and 0.40 (0.25−0.70) and 0.47 (0.34−0.80) for DEP0.18, respectively, in THP-1 and BEAS-2B cells. Our results implicate that potential risks of OS from above-critical exposure to DEP2.5 in all settings are found, whereas from DEP0.18 in the driver in northern Taiwan setting is also alarming.
Journal: Science of The Total Environment - Volume 387, Issues 1–3, 15 November 2007, Pages 113–127